παραλυτικός ειλεός

[kdiwavvou]

τι μπορεί να παρέχει ο γενικόσ ιατρός σε αυτή την περίπτωση ;

[kdiwavvou]

ομολογώ με θλίβει το γεγονός της μη τοποθέτησης των σεβαστών συναδέλφων

από τη μια αναλογίζομαι τις απόψεις επιφανών γενικών ιατρών ότι :

1. η ΠΦΥ κακώς έχει σχέση με το  επείγον, θα έπρεπε να υπάρχει φορέας  δίκην Ερυθρού Σταυρού όπως ήταν στην δεκαετία του '50
2. ο θάνατος είναι η φυσική εξέλιξη της ζωής, ας αφήσουμε τον άρρωστο να τελειώσει αξιοπρεπώς


από την άλλη σκέφτομαι τα εξής :

1. μια δύσκολη επιπλοκή δεν αφορά μόνο σε ασθενή τελικού σταδίου αλλά και σε υγιείς πληθυσμιακές ομάδες
2. πολλοί από εμάς ανανεώνουμε πιστοποιήσεις τύπου atls, apls, also και συναφή


εάν λοιπόν υποθετικά μιλώντας έχουμε τον εξοπλισμό και την εμπειρία  παρεμβαίνουμε όταν ο χρόνος δεν αποτελεί πολύτιμο βοηθό μας ;
off the laber  παρεμβατικές ενέργειες έχουν θέση στο επείγον όταν η κλινική εμπειρία θέτει την διάγνωση μιας απειλητιής για τη ζωή νοσσολογικής οντότητας ;

η αφορμή για αυτό το topic  ήταν η μελέτη γενικά περι της άννοιας και των νεοτέρων δεδομένων [= η άχρηστη πληροφορία της ημέρας ] και έπεσα σε υλικό σχετικά με την ακετλυλοχολίνη

    

Prokinetic Agents and Other Stimulants of GI Contractility

Direct activation of muscarinic receptors, such as with the older cholinomimetic agents (see Chapter 7), is not a very effective strategy for treating GI motility disorders because these agents enhance contractions in a relatively uncoordinated fashion that produces little or no net propulsive activity. By contrast, prokinetic agents are medications that enhance coordinated GI motility and transit of material in the GI tract. Although ACh, when released from primary motor neurons in the myenteric plexus, is the principal immediate mediator of muscle contractility, most of the clinically useful prokinetic agents act "upstream" of ACh, at receptor sites on the motor neuron itself, or even more indirectly, on neurons one or two orders removed from it. Although pharmacologically and chemically diverse, these agents appear to enhance the release of excitatory neurotransmitter at the nerve-muscle junction without interfering with the normal physiological pattern and rhythm of motility. Coordination of activity among the segments of the gut, necessary for propulsion of luminal contents, therefore is maintained.

Agents useful clinically in altering GI motility are considered below.

Cholinergic Agents

Choline Derivatives

The effects of ACh on smooth muscle are mediated in large part by two types of G protein–coupled muscarinic receptors (mAChRs), M2 and M3 (see Chapter 7 ), that are present in the GI tract in a 4:1 ratio, respectively. Although less abundant, the M3 receptor is more important; its activation increases intracellular Ca2+, an effect mediated by the Gq-PLC-IP3 pathway. ACh itself is not used pharmacologically because it affects all classes of cholinergic receptors (nicotinic and muscarinic) and is degraded rapidly by acetylcholinesterase. Modification of the structure of ACh has yielded drugs such asbethanechol that have increased receptor selectivity and that resist enzymatic hydrolysis. In addition to its lack of real prokinetic efficacy, bethanechol has significant side effects resulting from its broad muscarinic effects on contractility and secretion in the GI tract and other organs. These side effects include bradycardia, flushing, diarrhea and cramps, salivation, and blurred vision.

Acetylcholinesterase Inhibitors

These drugs inhibit the degradation of ACh by its esterase (see Chapter ,

thereby allowing ACh to accumulate at sites of release.

Unlike muscarinic receptor agonists, these parasympathomimetic drugs do not stimulate muscle directly, but rather accelerate GI transit times by enhancing the contractile effects of ACh released at synaptic and neuromuscular junctions.

Among these cholinergic muscle stimulants, neostigmine methylsulfate has been used off-label for some gastroenterological disorders,

particularly those associated with

acute colonic pseudo-obstruction (Ogilvie's syndrome) and
paralytic ileus.

The usual dose in the acute setting is 2 to 2.5 mg of neostigmine methylsulfate administered by IV push over 3 minutes

with continuous monitoring of ECG, blood pressure, and O2 saturation.
Atropine should be available in case of severe bradycardia (heart rate of less than 50 bpm).


βιβλιογραφική πηγή :
Goodman & Gilman's The Pharmacological Basis of Therapeutics, 11e 
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[EzeΤΡΟΛ]

γεια σου ρε φίλε από τη μια σε θαυμάζω 1. για την προσήλωσή σου σε καίρια ζητήματα [που αφορούν την ταμπακιέρα] από την άλλη υπάρχουν και

2. σημεία στίξης

ρε φίλoς να μας καταλαβαίνουνε τί λέμετε πωωωωω έκανα κεφάλι πάλι
να ΄σαι καλά να σε διαβάζουμε

πάθαμε μόρφωση πάλι τύφλα να΄χει η ταβανοσκόπηση
και οι άλλες μέθοδοι γκεστάλτ με τέτοια ποσταρίσματα που διαβάζουμε εδώ μέσα όλα τα $$ λουλούδια <δικόσ σου>

no hard feelings, eh?

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